New evidence on the neuropathological mechanisms of BMAA

Related case

Possible link between harmful algal blooms and β-N-methylamino-L-alanine (BMAA) neurotoxin

Algal blooms are on the rise worldwide, but no one has yet conducted comprehensive research to prove that they are a global phenomenon. β-N-methylamino-L-alanine (BMAA) is a neurotoxin with neurodegenerative effects, and recent studies suggest that it may play a role in the development of Alzheimer's disease and amyotrophic lateral sclerosis/Parkinson's disease (ALS/PDC). In 2003 it was described that cyanobacteria in water can also produce BMAA.

Read more »
In 2022 January a new review was published by Australian and Iranian researchers in Neurotoxicity Research about the neuropathological mechanism of BMAA.

The incidence of neurodegenerative diseases and cyanobacterial blooms is concomitantly increasing worldwide.

This new review evaluates different neuropathological mechanisms of BMAA at molecular and cellular levels and compares the related studies to provide some useful recommendations. Additionally, the structure and properties of BMAA as well as its microbial origin, especially by gut bacteria, are also briefly covered. Unlike previous reviews, the researchers hypothesize the possible neurotoxic mechanism of BMAA through iron overload. The BMAA may mediate in ferroptosis which results in the death of neuronal cells. BMAA-induced Fe overload can also cause cell damage in alternative ways (lipids, proteins, DNA and carbohydrates). Iron overload may also cause expression and aggregation of α-Syn (PD hallmark), and increase Aβ density and senile plaques formation (AD hallmark).

Related case

Newsletter subscription